Medical device for flow augmentation in patients with occlusive cerebrovascular disease and methods of use

ABSTRACT

The invention provides a medical device having first and second elongate tubular members. Each member comprises a manometer at a distal end and a lumen communicating with a port at the distal end. An expandable occlusive member is optionally mounted on either or both tubular members proximal to the distal port. A proximal end of each tubular member is adapted for attachment to an oxygenator and/or a pump for aspirating blood from an artery or a symptomatic carotid artery through the first tubular member and perfusing the blood into the contralateral carotid artery through the second tubular member, thereby providing a means of augmenting the collateral vasculature and maintaining perfusion distal to the offending lesion. The flow rate of blood can be controlled by inflating or deflating the balloon occluder. The device may employ a neuroprotective agent, hypothermic perfusion, and an atherectomy device or an extracorporeal pumping mechanism to remove a vascular occlusion and reestablish cerebral perfusion. Methods of using the devices in treating patients with acute stroke or occlusive cerebrovascular disease are also disclosed.

This is a divisional application of co-pending application Ser. No.09/232,438, filed Jan. 15, 1999, incorporated herein by reference in itsentirety.

FIELD OF THE INVENTION

The present invention generally relates to medical devices useful intreating patients with acute stroke or occlusive cerebrovasculardisease. More specifically, the invention provides an extra/intracranialdevice capable of removing blood from a peripheral artery or symptomaticcarotid artery and returning the blood to the contralateral carotidartery, thereby providing a means of augmenting the collateralvasculature and maintaining perfusion distal to the offending lesion.The device may employ neuroprotective agents, hypothermic perfusion, andan atherectomy device or an extracorporeal pumping mechanism to remove avascular occlusion and reestablish cerebral perfusion.

BACKGROUND OF THE INVENTION

Stroke is the third most common cause of death in the United States andthe most disabling neurologic disorder. Approximately 700,000 patientssuffer from stroke annually. Stroke is a syndrome characterized by theacute onset of a neurological deficit that persists for at least 24hours, reflecting focal involvement of the central nervous system, andis the result of a disturbance of the cerebral circulation. Outcomefollowing stroke is influenced by a number of factors, the mostimportant being the nature and severity of the resulting neurologicdeficit. The patient's age, the cause of stroke, and coexisting medicalillness also affect prognosis. Overall, less than 80% of patients withstroke survive for at least 1 month, and approximately 35% have beencited for the 10-year survival rates. Of patients who survive the acuteperiod, up to 75% regain independent function, while approximately 15%require institutional care.

Hemorrhagic stroke accounts for 20% of the annual stroke population.Hemorrhagic stroke often occurs due to rupture of an aneurysm orarteriovenous malformation bleeding into the brain tissue, resulting incerebral infarction. The remaining 80% of the stroke population arehemispheric ischemic strokes and are caused by occluded vessels thatdeprive the brain of oxygen-carrying blood. Ischemic strokes are oftencaused by emboli or pieces of thrombotic tissue that have dislodged fromother body sites or from the cerebral vessels themselves to occlude inthe narrow cerebral arteries more distally. When a patient presents withneurological symptoms and signs which resolve completely within 1 hour,the term transient ischemic attack (TIA) is used. Etiologically, TIA andstroke share the same pathophysiologic mechanisms and thus represent acontinuum based on persistence of symptoms and extent of ischemicinsult.

When a patient presents with neurological deficit, a diagnostichypothesis for the cause of stroke can be generated based on thepatient's history, a review of stroke risk factors, and a neurologicexamination. If an ischemic event is suspected, a clinician cantentatively assess whether the patient has a cardiogenic source ofemboli, large artery extracranial or intracranial disease, small arteryintraparenchymal disease, or a hematologic or other systemic disorder. Ahead CT scan is often performed to determine whether the patient hassuffered an ischemic or hemorrhagic insult. Blood would be present onthe CT scan in subarachnoid hemorrhage, intraparenchymal hematoma, orintraventricular hemorrhage.

Traditionally, emergent management of acute ischemic stroke consists ofmainly general supportive care, e.g. hydration, monitoring neurologicalstatus, blood pressure control, and/or anti-platelet or anti-coagulationtherapy. In June 1996, the Food and Drug Administration approved the useof Genentech Inc.'s thrombolytic drug, tissue plasminogen activator(t-PA) or Activase®, for treating acute stroke. In a randomized,double-blind trial, the National Institute of Neurological Disorders andt-PA Stroke Study, there was a statistically significant improvement instoke scale scores at 24 hours in the group of patients receivingintravenous t-PA within 3 hours of the onset of an ischemic stroke.Since the approval of t-PA, an emergency room physician could, for thefirst time, offer a stroke patient an effective treatment besidessupportive care.

However, treatment with systemic t-PA is associated with increased riskof intracerebral hemorrhage and other hemorrhagic complications.Patients treated with t-PA were more likely to sustain a symptomaticintracerebral hemorrhage during the first 36 hours of treatment. Thefrequency of symptomatic hemorrhage increases when t-PA is administeredbeyond 3 hours from the onset of a stroke. Besides the time constraintin using t-PA in acute ischemic stroke, other contraindications includethe following: if the patient has had a previous stroke or serious headtrauma in the preceding 3 months, if the patient has a systolic bloodpressure above 185 mm Hg or diastolic blood pressure above 110 mmHg, ifthe patient requires aggressive treatment to reduce the blood pressureto the specified limits, if the patient is taking anticoagulants or hasa propensity to hemorrhage, and/or if the patient has had a recentinvasive surgical procedure. Therefore, only a small percentage ofselected stroke patients are qualified to receive t-PA.

New devices and methods are thus needed in treating patients with acuteischemic stroke and occlusive cerebrovascular disease, in treatingsymptomatic patients with embolization or hemodynamic compromise, or instroke prevention, e.g., patients with incidental finding ofasymptomatic carotid lesion undergoing cardiothoracic surgery, whichimprove a patient's neurological function and quality of life withoutcausing significant side effect, and can be used in patients withcontraindication to using t-PA.

SUMMARY OF THE INVENTION

The invention provides devices and methods for treatment of acuteischemic stroke and occlusive cerebrovascular disease by takingadvantage of the collateral cerebral circulation. Anastomoses betweenthe cerebral arteries provide alternative pathways in which blood canreach a given region of the brain besides the predominant supplyingartery. At the base of the brain close to the sella turcica, circulusarteriosus cerebri, or Circle of Willis, connects the vertebral andinternal carotid arteries to each other and to the vessels of theopposite side. When occlusion of a blood vessel interrupting the flow ofblood to a specific region of the brain occurs, survival of the braintissue and therefore severity of a patient's neurological deficit dependon the number and size of its collateral arteries. Effective stroketherapies therefore rely on the physicians' ability to respond totreatment quickly, since the longer the brain is deprived of blood flow,the greater the damage that occurs. The devices and methods of thepresent invention are used to augment contralateral blood flow acrossthe Circle of Willis to improve and maintain perfusion to an ischemicregion distal to an occluded intra/extracranial cerebral artery, andthus can be utilized in stroke patients immediately after onset ofsymptoms to maintain viability of the cerebral tissue until theobstructing lesion is removed by an intervention or resolved with time(more than one half of the occluding thrombi usually lyse themselves ina few days).

One embodiment of the medical device comprises first and second elongatetubes. Each tube has a manometer at a distal end and a lumencommunicating with a port at the distal end. An expandable occlusivemember is optionally mounted on either or both tubular members proximalto the distal port and is adapted to expand to engage the lumen of anintracranial or extracranial artery. A proximal end of each tubularmember attaches to an oxygenator or a pump for aspirating blood throughthe first tube and perfusing the blood through the second tube.

In another embodiment, each tube has an additional lumen whichcommunicates with a port distal to the balloon occluder for infusingfluid and pharmaceutical agents, such as a neuroprotective agent orheparin.

In still another embodiment, the first and second tubes are carriedwithin the lumen of an elongate catheter. The lumen of either tubularmember communicates with one or a plurality of perfusion ports and isadapted for aspiration or infusion of blood.

In still another embodiment, the proximal end of either tubular memberincludes a blood filter which entraps any thromboembolic debris flowingthrough the circuit before blood is perfused to an artery.

In still another embodiment, the first tubular member, which is adaptedfor insertion into an occluded carotid or cerebral artery, comprises anadditional lumen adapted for introduction of an atherectomy device forremoving occlusive lesions in the artery.

The invention also provides methods for augmenting contralateralcirculation in a patient with occlusive cerebrovascular disease usingthe devices described above. The methods can be used to perfuse andmaintain blood flow to an ischemic region distal to an occluding lesionin patients who are symptomatic due to embolization of a cerebral arterylesion or hemodynamic compromise caused by the lesion. The methods canalso be used in stroke prevention, e.g., in asymptomatic patients whoare undergoing a major surgery such as cardiothoracic surgery and arefound incidentally to have significant flow limiting cerebral lesionsduring cardiac catheterization or angiogram.

In a first method, the distal end of the first tubular member isinserted through an incision into a peripheral artery, such as a femoralartery. The occluding lesion in the symptomatic artery is localized withan angiogram or intravascular ultrasound (IVUS). With assistance of aguide wire, the distal end of the second tubular member is insertedthrough the same incision or a different incision into the contralateralcarotid artery. Oxygenated blood is aspirated from the artery throughthe lumen and port of the first tubular member and perfused into thecontralateral carotid artery through the lumen and port of the secondtubular member. An expandable occluder, e.g., a balloon occluder, may beexpanded on the second tubular member proximal to the distal port tocontrol the flow rate more effectively. In this manner, augmentedcontralateral perfusion provides enhanced reversal of blood flow acrossthe Circle of Willis to compensate for the sudden decrease of flow inthe occluded artery.

In another method, the distal end of the first tubular member isinserted through an incision on a peripheral artery, such as a femoralartery, and advanced into the symptomatic carotid or cerebral arteryproximal to the occluding lesion. In an emergency, the device can alsobe inserted into a patient's carotid artery as a direct stick afterlocalizing the occlusion with the assistance of IVUS or standard carotiddoppler and/or transcranial doppler (TCD). The distal end of the tubularmember can be advanced as far as the occluding site which could be inthe common carotid artery, internal carotid artery, middle cerebralartery, anterior cerebral artery, carotid siphon, terminal internalcarotid artery, or any other part of the cerebral vasculature. Thedistal end of the second tubular member is then inserted through thesame incision or a different incision, and advanced into thecontralateral carotid artery. When present, the balloon occluder mountedon the first tubular member proximal to the distal port is inflated topartially occlude the arterial lumen. The proximal end of the firsttubular member is attached to a vacuum pump and blood is aspirated fromthe symptomatic carotid artery through the lumen and port of the firsttubular member, and delivered to the contralateral carotid arterythrough the lumen and port of the second tubular member. The flow ratecan be controlled by deflating or inflating the balloon, e.g., the flowrate increases as the balloon is deflated. The augmented contralateralhemispheric blood flow, which helps to reverse flow across the Circle ofWillis, provides (1) retrograde arterial collateral enhancement to theischemic area distal to the occlusion and (2) enhances the pressuredifferential across the occluding lesion, which may be sufficient todislodge any thromboembolic material. Blood aspirated from thesymptomatic artery is, in certain embodiments, passed through a bloodfilter optionally included in the proximal end of the first or secondtubular member or in the pump to entrap any embolic debris before theblood is returned to the contralateral carotid artery.

It will be understood that there are several advantages in using thedevices and methods disclosed herein for management of acute stroke. Forexample, the devices can be used (1) in a majority of stroke patients,including those with contraindication to using systemic t-PA, (2) toadminister neuroprotective agents locally into an occluded vessel,thereby providing greater local benefit and fewer systemic side effects,(3) to infuse hypothermic fluid or blood to the ischemic area, therebyproviding protective focal hypothermia, (4) with standard atherectomy toremove arterial atheroma, (5) as an angioplasty device by inflating theballoon over the stenotic arterial lumen to enlarge the luminaldiameter, (6) by any invasive radiologist or cardiologist, (7) in theangiogram or fluoroscopy suite available in most hospitals, (8) intreating acute stroke patients with few systemic side effects, (9) totreat symptomatic vertebral artery occlusion, (10) to maintain cerebralperfusion in patients with asymptomatic flow limiting carotid stenosisundergoing major cardiothoracic surgeries or in patients withhemodynamic instability, e.g., cardiogenic or septic shock, and (11) tomaintain perfusion to the distal ischemic area, even without removal ofthe occlusion, to minimize neurologic damage while alternativeintervention is being considered.

BRIEF DESCRIPTION OF THE DRAWINGS

FIG. 1 depicts a normal cerebral circulation in the Circle of Willis.

FIG. 2 depicts a reversed circulation in the Circle of Willis tocompensate for an occlusion in the left internal carotid artery.

FIG. 3A depicts an embodiment of the medical device for treatment ofacute stroke according to the present invention.

FIG. 3B depicts the device shown in FIG. 3A inserted in thecontralateral carotid artery.

FIG. 4 depicts another embodiment of the device inserted in the carotidartery to provide contralateral flow augmentation.

FIG. 5A depicts a distal region of another embodiment of the device fortreatment of acute stroke.

FIG. 5B depicts the device of FIG. 5A inserted into bilateral carotidarteries.

FIG. 6 depicts a distal region of another embodiment of the devicehaving a balloon occluder.

FIG. 7A depicts another embodiment of the device having two balloonoccluders.

FIG. 7B depicts a proximal region of the device shown in FIG. 7A.

FIG. 7C depicts a distal region of the device in FIG. 7A inserted in thecarotid arteries.

FIG. 8A depicts still another embodiment of the device having twoballoon occluders and a plurality of perfusion ports on one of thetubular members.

FIG. 8B depicts still another embodiment of the device having balloonoccluders and a plurality of perfusion ports on both tubular members.

FIG. 9 depicts the device of FIG. 8B inserted in the vertebral arteries.

FIG. 10 depicts different peripheral artery access sites for insertionof the device.

DETAILED DESCRIPTION

The cerebral circulation is regulated in such a way that a constanttotal cerebral blood flow (CBF) is generally maintained under varyingconditions. For example, a reduction in flow to one part of the brain,such as in acute stroke, may be compensated by an increase in flow toanother part, so that CBF to any one region of the brain remainsunchanged. More importantly, when one part of the brain becomes ischemicdue to a vascular occlusion, the brain compensates by increasing bloodflow to the ischemic area through its collateral circulation.

FIG. 1 depicts a normal cerebral circulation and formation of Circle ofWillis. Aorta 100 gives rise to right brachiocephalic trunk 82, leftcommon carotid artery (CCA) 80, and left subclavian artery 84. Thebrachiocephalic artery further branches into right common carotid artery85 and right subclavian artery 83. The left CCA gives rise to leftinternal carotid artery (ICA) 90 which becomes left middle cerebralartery (MCA) 97 and left anterior cerebral artery (ACA) 99. Anteriorly,the Circle of Willis is formed by the internal carotid arteries, theanterior cerebral arteries, and anterior communicating artery 91 whichconnects the two ACAs. The right and left ICA also send right posteriorcommunicating artery 72 and left posterior communicating artery 95 toconnect respectively with right posterior cerebral artery (PCA) 74 andleft PCA 94. The two posterior communicating arteries and PCAs, and theorigin of the posterior cerebral from basilar artery 92 complete thecircle posteriorly.

When occluding lesion 70 occurs acutely, for example, in left internalcarotid artery 90, as depicted in FIG. 2, blood flow in the rightcerebral arteries, left external carotid artery 78, right vertebralartery 76, and left vertebral artery 77 increases, resulting indirectional change of flow through the Circle of Willis to compensatefor the sudden decrease of blood flow in the left internal carotidartery. Specifically, blood flow reverses in right posteriorcommunicating artery 72, right PCA 74, and left posterior communicatingartery 95. Anterior communicating artery 91 opens, reversing flow inleft ACA 99, and flow increases in the left external carotid artery,reversing flow along left ophthalmic artery 75, all of which contributeto flow in left ICA 90 distal to the occluding lesion to provideperfusion to the ischemic area distal to the occlusion.

FIGS. 3A and 3B depict an embodiment of the device for treatment ofhemispheric ischemia. The device comprises first tubular member 1 andsecond tubular member 2. The first tubular member has lumen 10communicating with distal port 11 and proximal end 13 adapted foraspiration of blood. The second tubular member has lumen 20communicating with distal port 22 and proximal end 23 adapted forperfusion of blood. The first and second tubular members are carriedwithin a lumen of elongate catheter 33. Manometer 30, communicatingproximally with sensor attachment 31, is carried at distal end 24 of thesecond tubular member for measuring blood pressure at the distal end.Proximal end 13 of the first tubular member and proximal end 23 of thesecond tubular member are adapted for attachment to a pump oroxygenator.

In using the device of FIG. 3A for treatment of hemispheric ischemia,the device is inserted through an incision on a peripheral artery, suchas the left femoral artery shown in FIG. 3B. After localizing occludinglesion 70 in the left carotid artery with the assistance of IVUS orstandard carotid doppler and transcranial doppler (TCD), distal end 24of second tubular member 2 is advanced over a guide wire to position inthe right carotid artery. Distal end 14 of tubular member 1 can bepositioned in the descending aorta, the subclavian, the axillary, thefemoral, or the iliac artery as depicted in FIG. 3B. Proximal end 13 and23 are connected to pump 35, which aspirates blood from port 11 andlumen 10 of the first tubular member, delivering the blood through bloodfilter 36 included in pump conduit 37, and perfusing the blood to theright carotid artery through lumen 20 and port 22 of the second tubularmember. Heparin may be administered through either proximal end of thetubular members or the pump conduit to provide anticoagulation, therebypreventing thrombi forming in the circuit. In some instances, the pumpmay not be necessary. Increasing blood flow in the right carotid arteryresults in augmented flow in the right cerebral arteries and the rightvertebral artery, enhancing directional change of flow through theCircle of Willis to compensate for the sudden decrease of blood flow inthe left internal carotid artery as described in FIG. 2. This method isparticularly useful in situations in which increasing ipsilateralperfusion cannot be accomplished, e.g., in vessels having near total orcomplete occlusion. By increasing contralateral perfusion, someimprovement in a patient's neurologic function may be achieved.

FIG. 4 depicts another embodiment of the device inserted through twoseparate incisions on the left femoral artery. Tubular members 1 and 2may be inserted through the same incision or different incisions on theartery. Construction of this device and methods of using it are similarto those described in FIG. 3A except insofar as the tubular members arenot carried within a lumen of a catheter. This embodiment may bedesirable in situations in which the first tubular member is insertedinto a vein, such as the femoral, iliac, axillary or subclavian vein.Deoxygenated blood is aspirated through port 11 and lumen 14 anddelivered to an oxygenator. Oxygenated blood is then delivered to pump35 and to the right carotid artery through lumen 20 and port 22 toprovide contralateral perfusion augmentation to the ischemic cerebraltissue distal to occlusion 70. Mild to moderate hypothermia, atapproximately 32 to 34° C., can be introduced during the bloodrecirculation. Neuroprotective agents, administered to the contralateralcarotid artery through lumen 20 and port 22, may reach the ischemicregion more effectively.

FIGS. 5A and 5B depict still another embodiment of the device, whichcomprises tubular members 1 and 2. The first tubular member has lumen 10communicating with distal port 11 and proximal end 13 adapted foraspiration of blood from a carotid or a cerebral artery. The secondtubular member has lumen 20 communicating with distal port 22 andproximal end 23 adapted for perfusion of blood to a carotid artery. Thefirst and second tubular members are carried within a lumen of elongatecatheter 33. Manometer 30 and manometer 40 are carried respectively atdistal end 24 of the second tubular member and distal 14 of the firsttubular member for measuring blood pressure at the distal end. Bloodfilter 36 is included in the proximal end of the second tubular memberto capture embolic debris.

In use, the device is inserted through an incision on the left femoralartery as shown in FIG. 5B. The distal end of tubular member 1 isadvanced over a guide wire into the left carotid artery until occludinglesion 70 is localized with dye, and the distal end is positionedproximal to the occlusion. The distal end of tubular member 1 can beadvanced as far as the occluding site which could be in the commoncarotid artery, internal carotid artery, middle cerebral artery,anterior cerebral artery, carotid siphon, terminal internal carotidartery, or any other part of the cerebral vasculature. In an emergency,the device can also be inserted into a patient's carotid artery as adirect stick after localizing the occlusion with the assistance of IVUSor standard carotid doppler and transcranial doppler (TCD). The distalend of tubular member 2 is inserted into the right carotid artery,either the CCA or ICA. Proximal end 13 and 23 of the first and secondtubular member respectively are attached to pump 35. Blood is aspiratedfrom the occluded carotid artery through lumen 10 and port 11, anddelivered to the contralateral carotid artery through lumen 20 and port22 after it passes through blood filter 36 included in the proximal endof the second tubular member.

The perfusion rate is generally approximately between 7 and 800 cc/minand up to 1.2 liters/min. Heparinization is generally required toprevent thrombi forming in the flow circuit. Any embolic debris isfiltered with 100 to 200 micron filter 36 prior to reentry. Theaugmented contralateral hemispheric blood flow, which reverses flowacross the Circle of Willis via ACA, posterior communicating,ophthalmic, and external carotid arteries, provides not only retrogradearterial collateral enhancement to the ischemic area distal to theocclusion, but also enhanced pressure differential across the occlusion,which may be sufficient to dislodge and thereby remove the occludinglesion or any embolic debris in the symptomatic artery. The desired flowrate necessary to reverse flow across the Circle of Willis is modifiedaccording to the patient's physical examination, since the patient maydevelop “steal” symptoms. As blood is aspirated from the symptomaticcarotid artery, blood flow may be reduced significantly to result in“steal syndrome,” similar to “subclavian steal syndrome” in whichsignificant subclavian stenosis leads to blood flow reversal in thevertebral artery and is redirected away from the brain to the distalsubclavian artery with physical activity of the ipsilateral arm.Aspiration of blood is reduced or discontinued if ischemic symptomsensue.

The embodiment depicted in FIG. 6 differs from the embodiment depictedin FIG. 5B in that balloon occluder 50, communicating with inflationlumen 51, is mounted on distal region 24 of the second tubular memberproximal to port 22. In use, as the first tubular member is inserted inthe symptomatic carotid artery and the second tubular member is insertedin the contralateral carotid artery, the balloon can be inflated toocclude the arterial lumen to reduce run-off of perfused blood and toprovide compartmentalization for administration of pharmaceuticalagents, such as a neuroprotective agent.

FIGS. 7A and 7B depict, respectively, a distal and a proximal region ofanother embodiment of the device for treatment of acute stroke. Thedevice comprises first tubular member 1 and second tubular member 2. Thefirst and second tubular members are carried within a lumen of elongatecatheter 33. The first tubular member has lumen 10 communicating withdistal port 11 and proximal end 13. The second tubular member has lumen20 communicating with distal port 22 and proximal end 23. The proximalends of both tubular members are connected to pump 35 for aspiratingblood from the first tubular member and delivering it to the secondtubular member through conduit 37. Lumens 10 and 20 further communicate,respectively, with proximal ports 68 and 58, which can be used toadminister heparin or neuroprotective agents.

Blood filter 36 is included in the proximal end of the first tubularmember for capturing embolic material in the blood before returning tothe second tubular member. Manometer 30 communicating with sensorattachment 31 is carried at distal end 24 of the second tubular memberfor measuring blood pressure at the distal end. Likewise, manometer 40communicating with sensor attachment 32 is carried at distal end 14 ofthe first tubular member. Balloon occluder 50 communicating withinflation lumen 51 is mounted on the distal end of the second tubularmember proximal to port 22. Likewise, balloon occluder 60 communicatingwith inflation lumen 61 is mounted on the distal end of the firsttubular member proximal to port 11.

In use, distal end 14 of first tubular member 1 is inserted proximal tooccluding lesion 70 in the left carotid artery and distal end 24 ofsecond tubular member 2 is inserted in the right carotid artery as shownin FIG. 7C. Blood is aspirated from the occluded artery through port 11and lumen 10 of the first distal member, passed through the blood filterincluded in the proximal end of the first tubular member, and returnedto the contralateral artery through lumen 20 and port 22 via the pump.Balloon 50 on the second tubular member can be inflated to (1) preventrun-off of the perfused blood, (2) control flow rate to thecontralateral artery, e.g., the flow rate decreases as the balloon isdeflated, and (3) provide complete compartmentalization for moreefficacious administration of pharnacotherapy to the cerebral tissues.An atherectomy device may be introduced through an additional lumen (notshown) included in the first tubular member to remove the occludinglesion. Balloon 60 on the first tubular member can be inflated ordeflated to (1) control the flow rate of aspirated blood, e.g., the flowrate increases as the balloon is deflated, (2) increase negativepressure proximal to the occlusion, thereby enhancing the pressuregradient across the occlusion, which may dislodge the offending lesion,and (3) assist in removing tissue or atheromatous debris generatedduring atherectomy, thereby reducing embolization to the distalarteries.

FIGS. 8A and 8B depict still other embodiments of the device having aplurality of ports. The embodiments comprise balloon occluders 50 and60, communicating respectively with inflation lumen 51 and 61, mountedon first tubular member 1 and second tubular member 2. In FIG. 8A, lumen10 of the first tubular member communicates with port 11 distally. Lumen20 of the second tubular member communicates with 1, 2, 3, 4, 5, 6, orother number of perfusion ports 66 distally to provide more efficientdelivery of perfused blood to the contralateral carotid artery. In FIG.8B, lumens 10 and 20 of the first and second tubular memberscommunicate, respectively, with distal port 11 and 22, and with 1, 2, 3,4, 5, 6, or other number of perfusion ports 66 distally; in which casethe ports can be used to aspirate blood from the symptomatic carotidartery or perfuse blood to the contralateral carotid artery.

In patients with vertebral artery occlusions, treatment with angioplastyoften results in disastrous complications due to embolization of theocclusive lesion downstream to the basilar artery. Emboli small enoughto pass through the vertebral arteries into the larger basilar arteryare usually arrested at the top of the basilar artery where itbifurcates into the posterior cerebral arteries. The resulting reductionin blood flow to the ascending reticular formation of the midbrain andthalamus produces immediate loss or impairment of consciousness. Thedevices and methods described above can be used to (1) maintainperfusion to an ischemic region by enhancing blood flow to thecontralateral artery when ipsilateral perfusion can not be augmented,(2) remove thromboembolic material from the vertebral artery, or (2)provide protection during angioplasty and/or stenting by occluding theartery, reversing the flow and so preventing emboli from progressingthrough the basilar artery.

In using the device of FIG. 8A, for example, the occluding lesion isfirst localized with transcranial doppler or angiogram. Distal end 14 offirst tubular member 1 is shown inserted proximal to thromboembolicmaterial 70 in right vertebral artery 87 as shown in FIG. 9. Distal end24 of second tubular member 2 is inserted in left vertebral artery 88.Alternatively, distal end 14 can be inserted in the rightbrachiocephalic or the right subclavian artery, and distal end 24 can beinserted in the left subclavian or the left carotid artery. Proximalends of both tubular members are attached to a pump for aspirating bloodfrom the occluded vertebral artery and returning to the contralateralvertebral artery. Balloon occluders 50 and 60 can be inflated to controlthe flow rate. In this manner, perfusion to the ischemic area distal tothe occlusion is maintained by enhancing blood flow to the contralateralartery, thereby opening collateral arteries and reversing flow acrossthe Circle of Willis to the symptomatic vertebral artery. Alternatively,distal end 24 can be inserted in the ipsilateral carotid artery whenperfusion to the ischemic region via ipsilateral collaterals can beaugmented. By applying suction to the distal end of the first tubularmember, the pressure gradient across the occluding lesion increases andthromboembolic material 70 may be dislodged onto the distal port and beremoved. By using the devices and methods with an angioplasty oratherectomy device to remove a thromboembolic lesion in the vertebralartery, embolization from the vertebral distally to the basilar arterymay be minimized.

FIG. 10 depicts different sites of entry for the devices disclosedherein. An incision can be made on a peripheral artery, such as rightfemoral artery 122, left femoral artery 120, right radial artery 116,left radial artery 115, right brachial artery 112, left brachial artery110, right axillary artery 126, left axillary artery 115, rightsubclavian artery 142, or left subclavian artery. An incision can alsobe made on right carotid artery 132 or left carotid artery 130 inemergency situations.

The length of either tubular member will generally be between 10 and 200centimeters, preferably approximately between 30 and 150 centimeters.The inner diameter of the tubular member will generally be between 0.2and 0.7 centimeters depending on the desired perfusion rate, preferablyapproximately between 0.3 and 0.5 centimeters. The diameter of theexpanded occluder will generally be between 0.3 and 2 centimeters,preferably approximately 0.5 and 1.0 centimeters. The foregoing rangesare set forth solely for the purpose of illustrating typical devicedimensions. The actual dimensions of a device constructed according tothe principles of the present invention may obviously vary outside ofthe listed ranges without departing from those basic principles.

Although the foregoing invention has, for the purposes of clarity andunderstanding, been described in some detail by way of illustration andexample, it will be obvious that certain changes and modifications maybe practiced which will still fall within the scope of the appendedclaims.

What is claimed is:
 1. A medical device for augmenting contralateralcirculation in a patient having carotid stenosis, comprising: a firstelongate tubular member having a lumen communicating with a port at adistal end, a manometer carried at the distal end, and an expandableocclusive member carried proximal to the distal port and adapted toexpand and engage the lumen of a first carotid artery having a stenosis;a medical device extending through the first elongate tubular member toaccess the stenosis in the first carotid artery, wherein the medicaldevice is an atherectomy catheter; a second elongate tubular memberhaving a lumen communicating with a port at a distal end, a manometercarried at the distal end, and an expandable occlusive member carriedproximal to the distal port and adapted to expand and engage the lumenof a second carotid artery; and a pump connected to the proximal end ofthe first tubular member and the proximal end of the second tubularmember for aspirating blood through the first tubular member andperfusing the blood through the second tubular member.
 2. The medicaldevice of claim 1, wherein the port and lumen of each tubular member areadapted for infusion of fluid and pharmaceutical agents.
 3. The medicaldevice of claim 2, wherein the pharmaceutical agent is a neuroprotectiveagent.
 4. The medical device of claim 2, wherein the pharmaceuticalagent is heparin.
 5. The medical device of claim 1, wherein the secondtubular member further comprises an additional lumen and port forinfusion of fluid and pharmaceutical agent.
 6. The medical device ofclaim 1, wherein the first and second tubular members are carried withinthe lumen of an elongate catheter.
 7. The medical device of claim 1,wherein the proximal end of the first tubular member includes a bloodfilter.
 8. The medical device of claim 1, wherein the proximal end ofthe second tubular member includes a blood filter.
 9. The medical deviceof claim 1, wherein the lumen of the second tubular member communicateswith a plurality of perfusion ports.
 10. A medical device for augmentingcontralateral circulation in a patient having carotid stenosis,comprising: a first elongate tubular member having a lumen communicatingwith a port at a distal end, a manometer carried at the distal end, andan expandable occlusive member carried proximal to the distal port andadapted to expand and engage the lumen of a first carotid artery havinga stenosis; a second elongate tubular member having a lumencommunicating with a port at a distal end, a manometer carried at thedistal end, and an expandable occlusive member carried proximal to thedistal port and adapted to expand and engage the lumen of a secondcarotid artery; a medical device extending through the first elongatetubular member to access the stenosis in the first carotid artery,wherein the medical device is an atherectomy catheter; a pump connectedto the proximal end of the first tubular member and the proximal end ofthe second tubular member for aspirating blood through the first tubularmember and perfusing the blood through the second tubular member; and afilter carried by one of the first elongate tubular member or the secondelongate tubular member.
 11. The medical device of claim 10, wherein theport and lumen of each tubular member are adapted for infusion of fluidand pharmaceutical agents.
 12. The medical device of claim 10, whereinthe first and second tubular members are carried within the lumen of anelongate catheter.
 13. The medical device of claim 10, wherein the lumenof the second tubular member communicates with a plurality of perfusionports.
 14. A medical device for augmenting contralateral circulation ina patient having carotid stenosis, comprising: a first elongate tubularmember having a lumen communicating with a port at a distal end, amanometer carried at the distal end, and an expandable occlusive membercarried proximal to the distal port and adapted to expand and engage thelumen of a first carotid artery having a stenosis; a second elongatetubular member having a lumen communicating with a port at a distal end,a manometer carried at the distal end, and an expandable occlusivemember carried proximal to the distal port and adapted to expand andengage the lumen of a second carotid artery; a medical device extendingthrough the first elongate tubular member to access the stenosis in thefirst carotid artery, wherein the medical device is selected from thegroup consisting of an atherectomy catheter, an angioplasty catheter,and a stent catheter; a pump connected to the proximal end of the firsttubular member and the proximal end of the second tubular member foraspirating blood through the first tubular member and perfusing theblood through the second tubular member; and a third elongate tubularmember that carries the first elongate tubular member and secondelongate tubular member, and is slideable relative to the first elongatetubular member and second elongate tubular member.
 15. The medicaldevice of claim 14, wherein the port and lumen of each tubular memberare adapted for infusion of fluid and pharmaceutical agents.
 16. Themedical device of claim 15, wherein the pharmaceutical agent is aneuroprotective agent.
 17. The medical device of claim 15, wherein thepharmaceutical agent is heparin.
 18. The medical device of claim 14,wherein the second tubular member further comprises an additional lumenand port for infusion of fluid and pharmaceutical agent.
 19. The medicaldevice of claim 14, wherein the first and second tubular members arecarried within the lumen of an elongate catheter.
 20. The medical deviceof claim 14, wherein the first tubular member carries a blood filter.21. The medical device of claim 14, wherein the second tubular membercarries a blood filter.
 22. The medical device of claim 14, wherein thelumen of the second tubular member communicates with a plurality ofperfusion ports.